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EXPANDING LESIONS of the TEMPORAL FOSSA by LESLIE OLIVER, M.B.(Lond.), F.R.C.S., F.A.C.S

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EXPANDING LESIONS of the TEMPORAL FOSSA by LESLIE OLIVER, M.B.(Lond.), F.R.C.S., F.A.C.S Postgrad Med J: first published as 10.1136/pgmj.35.408.546 on 1 October 1959. Downloaded from 546 EXPANDING LESIONS OF THE TEMPORAL FOSSA By LESLIE OLIVER, M.B.(Lond.), F.R.C.S., F.A.C.S. Neurosurgeon: Charing Cross Group of Hospitals, Royal Northern Hospital, West End Hospital for Neurology and Neurosurgery, The French Hospital, London; and Southend General Hospital, Southend-on-Sea. Senior Neurosurgeon: North-East Regional Neurological and Neurosurgical Centre, Oldchurch Hospital, Romford, Essex Brain-stem Compression :ii.ii$iiliiiri; Expanding lesions in the temporal fossa readily ::I:. :: displace the brain-stem towards the opposite side iii.,iiiiiaiirl;illji.:;' .s.%.;.;.iig9l;;;"a.:·ii' where it is forced against the edge ofthe tentorium. ::·:: :1;·:: At the same time a wedge formed by the uncus and hippocampalgyrus is forced downward between the midbrain and the of the tentorium on the edge :i I.sapr .e side of the lesion (Fig. i). These two mechanisms produce the various stages of midbrain com- pression. The downward herniation of the uncus and hippocampal gyrus also compresses the homo- lateral oculomotor nerve. the ncrve is at copyright. Rarely :ig first stimulated and therefore the is con- pupil ::i:' but as on the nerve Y..i Lii stricted, pressure increases :!:. paralysis ensues and the pupil becomes dilated. ic?·i Usually, however, the pupil dilates as soon as the :';l..ss.l:·ii··:;.T.Rs. 't...i.li;C nerve is If the is conscious, compressed. patient :" i'lP ptosis and paralysis of the external ocular muscles ::i:;:"'··'·'!l:CiiUi%ii supplied by the oculomotor nerve may be observed. b :siai:.l:·:i·iiiiiir:::l The posterior cerebral artery prolapses through .s.".8.i.g.j.b,lSiiiiiiF·i ·:';i.ii..iiil!j.i.iii': il'.r"'e,· :ti:: the tentorial notch with the herniated brain and http://pmj.bmj.com/ a contralateral hemi- S:iliii4LtiiiiiC1;;ilii:,iii.ii :::i:' occasionally homonymous d:·*.·:1.::i i:;iiiiii.,ai:iiiii:!i:c.:·· anopia is produced by kinking of the artery or its calcarine branch over the free of the FIG. I.-Temporal lobe herniation. The groove made edge by the free edge of the tentorium on the under tentorium. surface of the left temporal lobe is indicated by Increased intracranial pressure is produced by arrows. The enlargement of the temporal lobe expansion of the lesion itself, pressure on the mid- was caused by a glioblastoma multiforme. (From brain and consequent obstruction of the aqueduct 'Basic Surgery' by kind permission of the of Sylvius, and often also by associated cerebral publishers, H. K. Lewis, London.) on October 2, 2021 by guest. Protected oedema. The increasing pressure, if not too rapid, may produce papilloedema. It also causes descent the side of the lesion, and contralateral or homo- of the brain-stem through the tentorial opening lateral hemiparesis with hypertonia, hyperreflexia sometimes resulting in sufficient traction on one or and a positive Babinski sign. (Homolateral both abducens nerves to cause unilateral or pyramidal signs are caused by displacement of the bilateral external rectus palsy. If descent of the brain-stem away from the side of the lesion and brain-stem continues, ' coning' of the cerebellar resulting indentation of the contralateral cerebral tonsils occurs at the foramen magnum and com- peduncle by the edge of the tentorium-the pression of the medulla oblongata results. Kernohan-Woltman phenomenon.) Occasionally Midbrain compression may be roughly classi- contralateral or homolateral Parkinsonian tremor fied into the following stages: and rigidity, presumably due to ischaemia of the Stage i. Clouding of consciousness, normal substantia nigra or its efferent pathways. pupils or occasionally contraction of the pupil on Stage 2. Stupor, dilatation and paralysis of the Postgrad Med J: first published as 10.1136/pgmj.35.408.546 on 1 October 1959. Downloaded from October 1959 OLIVER: Expanding Lesions of the Temporal Fossa 547 pupil on the side of the lesion (Hutchinson's pupil), Personality Changes and contralateral or homolateral hemiparesis, The temporal cortex is concerned with the hypertonia, and hyperreflexia with unilateral or reception, directly or indirectly, of association- bilateral Babinski responses. Occasionally Parkin- fibre systems of the other areas of the cerebral sonian manifestations in the limbs. Increasing cortex, and may therefore be expected to play an pulse rate (the classical slow pulse, although of important part in the total function of the cerebral considerable diagnostic importance, is found less cortex. Nevertheless, personality changes are often than a fast one). rarely associated with expanding lesions of the Stage 3. Coma, dilatation and paralysis of the temporal fossa, but when they do occur they take pupil on the side of the lesion or on both sides, the form of anxiety, irritability and occasionally decerebrate rigidity with increased tendon jerks agressiveness. This is in marked contrast with and bilateral Babinski responses. Cheyne-Stokes the apathy often produced by expanding lesions respiration. Tachycardia (if cerebellar coning of the anterior fossa. is causing compression of the medulla oblongata, the pulse may be slow and associated with in- Temporal Lobe Epilepsy creased blood pressure and slow respiration). About a quarter of all cases of epilepsy have their focus of discharge in one or other temporal Stage 4. Absence of response to all external lobe. Although atrophy of part of the temporal sensory stimuli, dilatation and paralysis of both lobe is the most commonly occurring underlying pupils, flaccidity of all voluntary muscles, absent pathological process, tumours account for a sig- tendon reflexes, bilateral Babinski responses or nificant proportion of cases of temporal lobe absent plantar reflexes. Rapid weak pulse. epilepsy. Often the discharge is confined to the Shallow slow respirations. temporal lobe, giving rise to characteristic Patients may pass from one stage to another in phenomena, but it may spread over the whole of either direction. Rapidly expanding lesions in the cerebral cortex to produce grand mal attacks. the temporal fossa may lead immediately to stages There are several modes of origin of or Thus there are often no or temporal 3 4. lateralizing epilepsy and each reflects one of the functions of copyright. localizing signs with acute lesions. the temporal lobe. The commonest is a sensa- tion in the abdomen, chest or throat (visceral Visual Field Defects aura) and is related to autonomic function. The The optic radiation sweeps widely forward in classical attack as originally described by the upper posterior part of the temporal lobe Hughlings Jackson, begins with a sensation of a before passing backward to the occipital cortex. bad smell or taste accompanied by smacking of the Thus lesions within the temporal lobe may invade lips and a ' dreamy state'; the origin of such the radiation from below, and as attacks is in the uncus, hippocampus or amygdala, optic light rays the location of olfactory and function. from above strike the lower part of the retina and gustatory http://pmj.bmj.com/ light rays from one side strike the opposite side of Other patients complain of unpleasant noises or a the retina, contralateral homonymous upper disturbance of equilibrium, sometimes so severe quadrantic field defects are produced. This is in that the patient is thrown to the ground (gyratory contrast with lesions within the parietal lobe, for epilepsy); sounds may seem unduly loud or soft; they invade the optic radiation from above and these attacks are related to the auditory and cause contralateral homonymous lower quadrantic equilibratory functions of the superior temporal field defects. A lesion arising in either situation convolution. Some patients experience sudden may eventually cut across the whole of the optic fear, anger or pleasure. There may be a sudden on October 2, 2021 by guest. Protected radiation and produce a complete contralateral feeling of familiarity with the surroundings, or the homonymous hemianopia. Involvement of the patient may feel that what is happening has taken optic radiation usually, through not invariably, place before (deja vu phenomenon). Sometimes indicates a destructive lesion within the cerebrum objects seem small and receding (micropsia), or rather than of its surface. large and near (macropsia). A vivid recollection compression of the past with its associated emotions may force its way into consciousness. Patients may carry Dysphasia out complicated acts unrelated to present events Nominal dysphasia may occur with lesions of but sometimes related to the sensory phenomena the superior temporal convolution of the dominant and tending to be aggressive (not to be confused hemisphere. Lesions which spread upwards and with post-epileptic automatism). Depersonaliza- backwards from the dominant temporal lobe may tion (a feeling of complete detachment from self), eventually cause total aphasia by destroying the and sometimes the related phenomenon of auto- speech centres of the parietal lobe. scopy (seeing an image of oneself in the external Postgrad Med J: first published as 10.1136/pgmj.35.408.546 on 1 October 1959. Downloaded from 548 POSTGRADUATE MEDICAL JOURNAL October 1959 environment), are sometimes experienced. These brain damage. Sometimes, however, an acute curious effects are related to the highest functional subdural haematoma is large and clinically in- levels of the temporal lobe. distinguishable from an extradural haematoma. Its bulk tends to be in the temporal fossa
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